Ventilator-Associated Systemic Inflammation

Abstract

Positive pressure ventilation is commonly applied in patients undergoing general anesthesia or requiring ventilatory support due to acute respiratory failure to assure adequate ventilation and gas exchange. Conventional mechanical ventilation frequently uses low positive end-expiratory pressure (PEEP) levels with high tidal volumes ranging between 10 and 15 ml/kg ideal body weight [1–4]. However, positive pressure ventilation alone or in combination with preexisting lung disease may under certain circumstances itself contribute considerably to lung injury including pneumothorax, alveolar edema, and alveolar rupture [5,6]. In addition to mechanical lung damage, it has been hypothesized that conventional mechanical ventilation can induce release of inflammatory mediators and thereby contribute to lung injury [7]. Experiments in different animal models have demonstrated that mechanical stress to lung cells due to injurious mechanical ventilation using high tidal volumes and low levels of PEEP can aggravate preexisting lung inflammation resulting in increased alveolar and systemic levels of pro- and anti-inflammatory mediators [8’10]. In patients with acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) higher systemic and intra-alveolar levels of pro-inflammatory cytokines have been observed in recent investigations during mechanical ventilation with low PEEP and high tidal volumes [11–13]. In contrast, mechanical ventilation with moderate to high levels of PEEP and low tidal volumes of about 6 ml/kg ideal body weight has been suggested to prevent tidal collapse and overdistension of lung units.